C h a p t e r 2 2
Respiratory Tract Infections, Neoplasms, and Childhood Disorders
543
If the virus spreads to the lower respiratory tract, the
infection can cause severe shedding of bronchial and
alveolar cells. In addition to compromising the natural
defenses of the respiratory tract, influenza infection pro-
motes bacterial adhesion to epithelial cells.
Manifestations
In the early stages, the symptoms of influenza often are
indistinguishable from other viral infections. There is an
abrupt onset of fever and chills; malaise; muscle aching;
headache; profuse, watery nasal discharge; nonproductive
cough; and sore throat.
15–17
One distinguishing feature of
an influenza viral infection is the rapid onset, sometimes
in as little as minutes, of profound malaise. The symp-
toms of uncomplicated rhinotracheitis usually peak by
days 3 to 5 and disappear by days 7 to 10. Weakness,
cough, and malaise may persist for weeks after clinical
resolution of influenza. Young children with influenza
viral infection can have initial symptoms mimicking bac-
terial sepsis with high fevers and febrile convulsions.
Viral pneumonia occurs as a complication of influ-
enza, most frequently in the elderly or in persons with
cardiopulmonary disease, but has been reported in
pregnant women and in healthy, immunocompetent
people.
18
It typically develops within 1 day after onset
of influenza and is characterized by rapid progression
of fever, tachypnea, tachycardia, cyanosis, and hypo-
tension. The clinical course of influenza pneumonia
progresses rapidly. It can cause hypoxemia and death
within a few days of onset. Survivors often develop dif-
fuse pulmonary fibrosis.
Secondary complications typically include sinusitis,
otitis media, bronchitis, and bacterial pneumonia.
15
Persons who develop secondary bacterial pneumonia
usually report that they were beginning to feel better
when they experienced a return of fever, shaking chills,
pleuritic chest pain, and productive cough. The most
common causes of secondary bacterial pneumonia are
S. pneumoniae, S. aureus, H. influenzae,
and
M. catarrhalis.
This form of pneumonia commonly produces less cya-
nosis and tachypnea and is usually milder than primary
influenza pneumonia. Influenza-related deaths can result
from pneumonia as well as exacerbations of cardiopul-
monary conditions and other disease. Reye syndrome
(fatty liver with encephalitis) is a rare complication of
influenza, particularly in young children who have been
given aspirin as an antipyretic agent.
15
Diagnosis andTreatment
Diagnosis is based on symptoms such as sudden onset of
fever, cough, weakness, and myalgias. The probability
of influenza varies with the prevalence of the disease in
Hemagglutinin
Neuraminidase
Nucleoprotein
Polymerase
Viral envelope
RNA
A
B
C
FIGURE 22-2.
Influenza type A virus.
(A)
Model of the RNA influenza A virus, showing the
hemagglutinin and neuraminidase envelope glycoproteins that provide access to host cells.
(B)
Negative-stained transmission electron micrograph (TEM) depicting the ultrastructural details
of a number of influenza viral particles, or “virions.”
(C)
TEM revealing ultrastructural features
of the 1918 influenza pandemic virus virions. (B and C from the Centers for Disease Control and
Prevention Public Health Image Library. Nos. 8432, 8996. B courtesy of F.A. Murphy; C courtesy of
Cynthia Goldsmith.)
